Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cystic fibrosis (CF) is caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). The principal manifestations of CF include increased concentration of Cl- in exocrine gland secretions, pancreatic insufficiency, chronic lung disease, intestinal blockage and malabsorption of fat, and male and female infertility. Insight into the function of CFTR can be gained by correlating its cell-specific expression with the physiology of those cells and with CF pathology. Determination of CFTR messenger RNA in rat tissues by in situ hybridization shows that it is specifically expressed in the ductal cells of the pancreas and the salivary glands. In the intestine, decreasing gradients of expression of the CFTR gene are observed on both the crypt-villus and the proximal-distal axes. This expression is consistent with CFTR being responsible for bidirectional Cl- transport, secretion in the intestinal crypts and reabsorption in the silivary gland ducts, and suggests that in these tissues CFTR functions as a regulated Cl- channel. In the lung, a broad band of hybridization includes the mucosa and submucosa of the bronchi and bronchioles. In the testis, CFTR expression is regulated during the cycle of the seminiferous epithelium. Postmeiotic expression is maximal in the round spermatids of stages VII and VIII, suggesting that CFTR plays a critical role in spermatogenesis and that deficiency of this function contributes to CF male infertility.
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PMID:In vivo cell-specific expression of the cystic fibrosis transmembrane conductance regulator. 171 39

The present study was undertaken in view of the higher incidence of thromboembolism in patients with Crohn's disease. The blood coagulation system was studied in 12 patients previously operated for Crohn's disease (8 cases of ileitis, 4 cases of colitis) and followed as out-patients. In 75% of cases, the disease was in an inactive stage. Eight patients showed slight lipid malabsorption. Serum levels of fibrinogen, platelets and factor V were shown to be significantly increased (p less than 0.001) as compared to controls. Prothrombin time and factors II, VII and X were shown to be decreased, while factors VIII and IX and antithrombin III were not significantly altered. Thrombocytosis and hyperfibrinogenemia, as reported in literature, seem to determine a condition of blood hypercoagulability, playing therefore a primary pathogenetic role in the genesis of thromboembolism in patients with Crohn's disease.
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PMID:Blood coagulation alterations and thromboembolism in Crohn's disease. 664 10

It is generally accepted that human T-cell lymphotropic virus type III (HTL VIII) is the causative agent of acquired immunodeficiency syndrome (AIDS), but, asyet, there are no clear reasons for the different clinical manifestations of AIDS among individuals. In this article Douglas Archer and Walter Glinsmann discuss the history of AIDS and propose a link between HTLV-III infection and gastrointestinal disease processes with attendant malabsorption. They further propose that maximizing the nutritional status and minimizing the incidence of gastrointestinal infection of individuals infected with HTLV-III may prevent development of the full-blown AIDS.
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PMID:Enteric infections and other cofactors in AIDS. 2529 Jul 77